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Biomedical subjects

J E Muller

Publications and source records attributed to J E Muller.

At least 91 records · Page 5Linked to original sources
PubMed1992

Pathophysiology and triggers of acute myocardial infarction: clinical implications.

A new approach to identification of the triggering mechanisms of acute myocardial infarction has been provided by the observation that the disease occurs more frequently during the morning hours compared to other times of day. This circadian variation results primarily from an increased relative risk during the initial 2-3 h after awakening and arising. The precise relationship between the onset of myocardial infarction and external factors such as activity and meal patterns needs to be determined in controlled epidemiologic studies. The possible underlying pathophysiologic mechanisms responsible for the circadian pattern of myocardial infarction include acute variations of blood pressure, heart rate, platelet aggregability and fibrinolytic activity, leading to an increased risk of plaque rupture and intracoronary thrombosis. Clinical implications of these findings include the need to design preventive regimens to provide maximum protection at the time of peak risk of myocardial infarction.

Adrenergic beta-Antagonists↗
PubMed1992

Triggering and hourly variation of onset of arterial thrombosis.

Information obtained during the past decade suggests that the onset of myocardial infarction and sudden cardiac death is frequently triggered by daily activities. The importance of physical or mental stress in triggering coronary thrombosis is supported by finding that (1) the frequencies of the onset of myocardial infarction, sudden cardiac death, and stroke show marked circadian variations, with similar increases in the period from 6 AM to noon; (2) the frequency of transient myocardial ischemia shows a similar increase in the morning, and episodes are often preceded by mental or physical triggers; (3) a ruptured atherosclerotic plaque, often nonobstructive by itself, lies at the base of most coronary thrombi; (4) a number of physiologic processes that could lead to plaque rupture, a hypercoagulable state, or coronary vasoconstriction, are accentuated in the morning; and (5) aspirin and beta-adrenergic blocking agents that affect certain of these processes have been shown to prevent disease onset. The hypothesis presented is that occlusive coronary thrombosis occurs when (1) an atherosclerotic plaque becomes vulnerable to rupture; (2) mental or physical stress causes the plaque to rupture; and (3) increases in coagulability or vasoconstriction, triggered by daily activities, contribute to complete occlusion of the coronary artery lumen. Recognition of the circadian variation--and the possibility of frequent triggering--of the onset of acute disease suggests the need for pharmacologic protection of patients during the vulnerable periods and provides clues to the mechanism of disease onset, the investigation of which may lead to improved methods of prevention.

Arteriosclerosis↗
PubMed1992

Platelet alpha 2 adrenoceptor characteristics during the morning increase in platelet aggregability.

The incidence of myocardial infarction and sudden cardiac death increases in the morning, as do platelet aggregability and sympathetic activity. We considered the possibility that increased platelet aggregability in the morning was due to an increase in platelet alpha 2 adrenergic receptor number or agonist binding affinity, or to a temporal disparity between the increase in sympathetic activity that accompanies arising and the anticipated decrease in platelet high affinity alpha 2 adrenoceptors. To evaluate these possibilities, we studied eight healthy male volunteers (20-35 years) before and 1-1.5 and 3-4 h after they arose at 08.00 h and performed routine morning activities. Platelet aggregability was determined in platelet-rich plasma; alpha 2 adrenoceptor density and agonist binding affinity were determined in intact platelets and in membrane preparations using the alpha 2 selective ligand [3H]-yohimbine. The threshold concentration of epinephrine required to produce biphasic aggregation decreased (i.e. platelet aggregability increased) from 3.6 +/- 1.2 to 0.9 +/- 0.3 microM (P less than 0.05) after arising. However, alpha 2 adrenoceptor density (380 +/- 71 to 365 +/- 51 sites per platelet) and agonist binding affinity assessed simultaneously did not change after arising, suggesting that the increase in platelet aggregability is due to factors extrinsic to the platelets or to an intra-platelet mechanism distal to the receptor level.

Adenosine Diphosphate↗
PubMed1991

Prognostic significance of the Karnofsky Performance Status score in patients with acute myocardial infarction: comparison with the left ventricular ejection fraction and the exercise treadmill test performance. The MILIS Study Group.

The prognostic significance of functional status has not been previously studied in the setting of acute myocardial infarction. We assessed the Karnofsky Performance Status (KPS) score, a simple functional status scale that is commonly used to categorize physical ability, in 849 patients with acute myocardial infarction who were enrolled in the Multicenter Investigation of the Limitation of Infarct Size (MILIS) study. We then compared the KPS score with other predictors of prognosis in these patients. In patients who presented with acute myocardial infarction, a lower KPS score (less than 8 on a scale of 1 to 10) 3 weeks before the index infarction was associated with a higher incidence of congestive heart failure, in-hospital cardiac arrest, and mortality during hospitalization, as compared with patients with KPS scores greater than or equal to 8 (each p less than 0.001). Cumulative 1-year and 4-year mortality rates were significantly higher in patients with KPS scores less than 8, as compared with patients with KPS scores greater than or equal to 8 (42.5% vs. 12.6% at 1 year and 61.6% vs 25.1% at 4 years, respectively; both p less than 0.001). The left ventricular ejection fraction on admission was significantly lower in patients with KPS scores less than 8, as compared with those with KPS scores greater than or equal to 8 (p less than 0.019). The cumulative mortality rate was equally well predicted by low KPS score and by left ventricular ejection fraction (both p less than 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)

Disability Evaluation↗
PubMed1991

The effect of enteric-coated aspirin on the morning increase in platelet activity.

In vitro platelet aggregability to adenosine diphosphate (ADP) and epinephrine increases in the morning, as does the frequency of myocardial infarction. A single-blind, randomized, cross-over study of 15 healthy males was conducted to determine: (1) if other measures of platelet activity show a morning increases and (2) if aspirin eliminates any increases in platelet activity detected. Subjects received 325 mg of enteric-coated aspirin (ECA) or placebo. During placebo therapy,platelet thromboxane A2 production (following collagen stimulation) increased significantly after the subjects got up, as did platelet aggregability to ADP, epinephrine, and collagen. ECA markedly reduced baseline platelet thromboxane A2 production and eliminated the increase after the subjects got up. It also abolished biphasic aggregation in response to epinephrine and ADP (thereby eliminating the morning increase in aggregability to these agents), lengthened collagen lag time, reduced synergistic aggregation to combined agonists, was effective on day 2, and did not alter increases of tissue plasminogen activator that occurred following the subjects' arising. If aspirin prevents myocardial infarction by its antiplatelet action, as seems likely, the preferential reduction of morning infarction observed in the Physicians' Health Study, and the demonstration that aspirin eliminates the morning increase in platelet activity, suggest that the morning increase in myocardial infarction is due in part to a concurrent relatively modest increase in platelet activity.

Adult↗
PubMed1991

Aspirin, platelet aggregation, and the circadian variation of acute thrombotic events.

The onset of several acute cardiovascular diseases occurs in a circadian pattern, with a peak incidence in the hours soon after awakening. This finding, coupled with laboratory data that confirm a surge in platelet activation during the early morning hours, suggests that acute changes in platelet aggregability may be an important trigger of thrombosis. Therefore, the efficacy of antiplatelet agents, such as aspirin, in reducing risks of vascular occlusion may result, at least in part, from a blunting of these short-term changes in platelet aggregability. In this review, clinical and laboratory evidence describing these cyclical changes is discussed, as is current evidence of the effects of aspirin on platelet function and the circadian variation of acute thrombosis.

Aspirin↗
PubMed1990

Time of onset of symptoms of acute myocardial infarction.

Several studies have observed an increased occurrence of acute myocardial infarction (AMI) in the morning based on subjective self-reports and objective confirmation. Evidence has also been collected to suggest a circadian variation in the onset of sudden cardiac death and silent myocardial ischemia. No published reports have examined the time of onset of AMI in relation to time after awakening. The present study examines the times of onset of AMI in relation to awakening in 137 patients with confirmed AMI. Information concerning time of awakening on the day of AMI revealed a marked increase in the onset of initial AMI symptoms within the first hour after awakening. Of the patients studied, approximately 23% reported onset of the initial symptoms of AMI within 1 hour after awakening. An increased onset of symptoms of AMI soon after awakening was also observed when patients in whom the acute cardiac symptoms were known to or may have caused awakening were excluded from consideration. This was also noted in subgroups of AMI patients classified according to age, order and location of AMI. These results extend previous observations of the circadian morning increase of AMI onset and assist in narrowing the search for potential triggers of the circadian variation of onset of AMI to physiologic changes that may occur soon after awakening.

Adult↗
PubMed1990

Analysis of possible triggers of acute myocardial infarction (the MILIS study).

Recent documentation of a circadian variation in acute myocardial infarction (AMI) suggests that AMI is not a random event, but may frequently result from identifiable triggering activities. The possible triggers reported by 849 patients enrolled in the Multicenter Investigation of Limitation of Infarct Size were analyzed. Possible triggers were identified by 48.5% of the population; the most common were emotional upset (18.4%) and moderate physical activity (14.1%). Multiple possible triggers were reported by 13% of the population. Younger patients, men and those without diabetes mellitus were more likely to report a possible trigger than were older patients, women and those with diabetes. The likelihood of reporting a trigger was not affected by infarct size. This study suggests that potentially identifiable triggers may play an important role in AMI. Because potential triggering activities are common in persons with coronary artery disease, yet infrequently result in AMI, further studies are needed to identify (1) the circumstances in which a potential trigger may cause an event, (2) the specific nature of potential triggering activites, (3) the frequency of such activities in individuals who do not develop AMI and (4) the presence or absence of identifiable triggers in various subgroups of patients with infarction.

Aged↗
PubMed1990

Spironolactone in the management of congestive heart failure.

Although many new drugs useful in the treatment of congestive heart failure have been introduced during the past 25 years, spironolactone continues to have an important role in the management of this condition. Spironolactone adds to the activity of the thiazide and loop diuretics to enhance the elimination of sodium and water. Furthermore, unwanted electrolyte disturbances such as hypokalemia and hypomagnesemia, associated with the administration of other classes of diuretics, can be minimized with spironolactone.

Diuretics↗
PubMed1990

Circadian variation of acute myocardial infarction and the effect of low-dose aspirin in a randomized trial of physicians.

Increased platelet aggregation in the morning and upon assuming an upright posture may account at least in part for the observed circadian variation in onset of acute myocardial infarction. The Physicians' Health Study, a randomized, double-blind, placebo-controlled trial of alternate-day aspirin intake (325 mg) among 22,071 US male physicians, afforded the opportunity to assess this circadian pattern and examine whether it is altered by aspirin therapy. During a 5-year period of follow-up, 342 cases of nonfatal myocardial infarction were confirmed, of which the time of onset was available in 211 (62%). The placebo group showed a bimodal circadian variation in onset of myocardial infarction with a primary peak between 4:00 AM and 10:00 AM (p less than 0.001). In the aspirin group, however, this circadian variation was minimal (p = 0.16), due primarily to a marked reduction in the morning peak of infarction. Specifically, aspirin was associated with a 59.3% reduction in the incidence of infarction during the morning waking hours, compared with a 34.1% reduction for the remaining hours of the day. The greater reduction was observed during the 3-hour interval immediately after awakening, a period with a risk of infarction twice that of any other comparable time interval (p less than 0.001). Aspirin intake was associated with a mean reduction in the incidence of infarction of 44.8% over the entire 24-hour cycle. These data support the hypothesis that increased platelet aggregability in the morning and upon arising contributes to the occurrence of myocardial infarction and that aspirin reduces the risk of infarction by inhibiting platelet aggregation during these critical periods.

Adult↗
PubMed1989

Probable triggers of onset of acute myocardial infarction.

Three cases of acute myocardial infarction are presented in which a probable triggering mechanism can be identified. The presence of triggering physical and mental stresses is consistent with recent documentation of a morning increase in frequency of acute myocardial infarction. This documentation suggests that the onset of acute myocardial infarction is not a random event. Recent advances in knowledge of the pathophysiology of acute myocardial infarction provide a background to the understanding of the probable triggering mechanism in these three cases. Further prospective study of patients with acute myocardial infarction in whom detailed information is collected sufficient to identify triggering activities may provide important insight into the pathophysiology of myocardial infarction and improved strategies for prevention.

Adult↗
PubMed1989

Ventricular septal and free wall rupture complicating acute myocardial infarction: experience in the Multicenter Investigation of Limitation of Infarct Size.

Left ventricular rupture was studied in 849 patients enrolled in the Multicenter Investigation of Limitation of Infarct Size. Although documented rupture occurred in only 14 cases (1.7%), it accounted for 14% of in-hospital mortality. Seven of the 14 ruptures occurred within 2 days and 10 within 4 days of the MB-creatine kinase-determined onset of infarction. Three easily determined baseline characteristics defined a set of patients with a markedly increased risk of myocardial rupture. Rupture was 9.2 times more likely to occur in patients with all of the following characteristics than in the remaining patients: (1) no history of previous angina or myocardial infarction, (2) ST segment elevation or signs of Q wave development on the initial ECG, and (3) peak MB-creatine kinase value (greater than or equal to 150 IU/L). The risk of myocardial rupture with these three characteristics was 5.5%. Although these predictors are likely to be of little therapeutic value for free wall rupture, since most patients with that complication die within minutes of its onset, they may aid in alerting physicians to the early diagnosis and timely surgical correction of ventricular septal rupture.

Creatine Kinase↗
PubMed1989

Pericarditis in acute myocardial infarction: characterization and clinical significance.

To determine the significance of pericarditis following acute myocardial infarction, the hospital course and 12-month follow-up were analyzed in 703 patients enrolled in the Multicenter Investigation of the Limitation of Infarct Size (MILIS). Pericarditis, defined by the detection of a pericardial rub, occurred in 20% of the patients (n = 141) and was more likely to follow Q wave than non-Q wave infarction (25% vs 9%, p less than 0.001). Patients with pericarditis experienced more serious myocardial damage compared to those without pericarditis, as evidenced by a larger infarct size (25 +/- 1 vs 17 +/- 1 MB-CK gm-Eq/m2, p less than 0.001), a lower admission left ventricular ejection fraction (42 +/- 1% vs 48 +/- 1%, p less than 0.001), and a higher incidence of congestive heart failure (47% vs 26%, p less than 0.001) and atrial tachyarrhythmias (16% vs 10%, p less than 0.05). When patients were classified by the presence of Q or non-Q wave infarction, these differences persisted although statistical significance was not always achieved due to smaller sample size. Mortality at 12-month follow-up for patients with pericarditis was 18% compared with 12% for patients without pericarditis (p = 0.055). This mortality difference could be accounted for in part by the lower ventricular ejection fraction in patients with pericarditis (p = 0.20 after adjustment).

Electrocardiography↗